Hepatitis C virus protease NS3/4A cleaves mitochondrial antiviral signaling protein off the mitochondria to evade innate immunity.

By Xiao-Dong Li, Lijun Sun, Rashu B. Seth, Gabriel Pineda, Zhijian J. Chen. Proceedings of the National Academy of Sciences of the United States of America, 2005

877 citations recorded by the source corpus.

Subfields: Cardiology and Cardiovascular Medicine, Hepatology, Immunology

View Paper: https://www.semanticscholar.org/paper/82903c943fd115068beeefdabf2e5ba0298c2484

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cardiology and Cardiovascular Medicine

1. Shizuo Akira
2. R. Randall
3. S. Goodbourn

In Hepatology

1. Shizuo Akira
2. Brett D. Lindenbach Heinz-J
3. O. Takeuchi
4. Charles M. Rice
5. R. Randall
6. S. Goodbourn

In Immunology

1. Shizuo Akira
2. Zhijian J. Chen
3. O. Takeuchi
4. S. Ghosh
5. Satoshi Uematsu
6. A. West
7. Taro Kawai
8. R. Randall

Citations in the corpus

• Anti-immunology: evasion of the host immune system by bacterial and viral pathogens. (2006, background): “…pathways are documented for poxviruses (Harte et al., 2003; DiPerna et al., 2004; Stack et al., 2005) and Hepatitis A & C viruses (Breiman et al., 2005; Fensterl et al., 2005; Foy et al., 2005; Li et al., 2005a, 2005b; Sumpter et al., 2005), but likely many other examples remain to be uncovered.”
• The specific and essential role of MAVS in antiviral innate immune responses. (2006, background): “…importance of the mitochondrial localization of MAVS is underscored by the recent discovery that hepatitis C virus (HCV) employs a serine protease, NS3/4A, to cleave MAVS off the mitochondrial membrane, thereby blocking interferon induction by the viral RNA (Li et al., 2005; Meylan et al., 2005).”
• Flaviviridae :T he Viruses and Their Replication (2007, background): “First, NS34A cleaves and inactivates the mitochondrial outer membrane protein alternately known as IPS-1, MAVS, VISA, or Cardif (397,486).”
• Cytosolic Sensing of Viruses (2013, background): “In addition, MAVS can be cleaved off mitochondria by the serine protease NS3-4A of HCV (Flaviviridae) and the ABC cysteine protease of hepatitis A virus (Picornaviridae) (Li et al., 2005; Meylan et al., 2005).”
• Innate Immunity to Virus Infection (2009, background): “IPS-1 is known to be cleaved by the HCV protease NS3 ⁄ 4A in HCV-infected cells (41, 46).”
• MAVS Forms Functional Prion-Like Aggregates To Activate and Propagate Antiviral Innate Immune Response (2011, background): “The importance of the mitochondrial localization of MAVS is underscored by the fact that hepatitis C virus employs the viral protease NS3/4A to cleave MAVS off the mitochondrial membrane, thereby suppressing type I interferon production (Li et al., 2005; Meylan et al., 2005).”
• Interferons and viruses: an interplay between induction, signalling, antiviral responses and virus countermeasures. (2008, background): “Recruited IRF-7 is phosphorylated by IRAK-1 in a TBK/IKKe-independent manner and translocates into the nucleus (still in association with MyD88, TRAF6 and IRAK-1), where it can bind to DNA and stimulate transcription.”
• Mitochondria in innate immune responses (2011, background): “For example, hepatitis C virus encodes a serine protease, termed NS3–4A, that inhibits RLR signalling and IFNβ production by cleaving MAVS from the OMM and preventing the formation of MAVS–IKKɛ signalling complexe”